I. Field of the Invention
The present invention relates generally to the field of cardiac rhythm management devices, including atrial, ventricular, and dual chamber pacemakers. More specifically, the present invention relates to a method and apparatus for attenuating polarization voltages or "afterpotentials" which develop at the heart tissue/electrode interface following the delivery of a stimulus to the heart tissue. The present invention allows accurate detection of an evoked response of the heart, to thereby determine whether each stimulus resulted in heart capture or contraction. The present invention further facilitates improved tracking of the capture threshold for minimizing power consumption while assuring therapeutic efficacy.
II. Discussion of the Prior Art
Cardiac pacers have enjoyed widespread use and popularity through time as a means for supplanting some or all of an abnormal heart's natural pacing functions. Among the various heart abnormalities remedied by pacemakers include total or partial heart block, arrhythmias, myocardial infarctions, congestive heart failure, congenital heart disorders, and various other rhythm disturbances within the heart. The fundamental components of a cardiac pacemaker include an electronic pulse generator for delivering stimulus pulses to the heart and an electrode lead arrangement (unipolar or bipolar) for sensing evoked responses from the heart. Cardiac pacemakers may be categorized generally as either external or implantable. External cardiac pacemakers are characterized as having the electronic pulse generator which resides outside the body with one or more electrode leads passing through the skin and ultimately into the heart for delivering pacing stimulus pulses and sensing evoked responses. Such external pacemakers are typically employed for temporary pacing, such as following a heart attack or open heart surgery, and are removed when no longer needed. Implantable pacemakers are used for long-term pacing and are characterized as having both the electrical pulse generator and electrode lead arrangement surgically implanted within the body of the patient. Depending upon the heart abnormality, cardiac pacemakers may be designed to engage in ventricular pacing, atrial pacing, or dual chamber pacing in both the atrium and ventricle.
Regardless of which type of cardiac pacemaker is employed to restore the heart's natural rhythm, all operate to stimulate excitable heart tissue cells adjacent to the electrode of the pacing lead employed with the pacemaker. Myocardial stimulation or "capture" is a function of the positive and negative charges found in each myocardial cell within the heart. More specifically, the selective permeability of each myocardial cell works to retain potassium and exclude sodium such that, when the cell is at rest, the concentration of sodium ions outside of the cell membrane is approximately equal to the concentration of potassium ions inside the cell membrane. However, the selective permeability also retains other negative particles within the cell membrane such that the inside of the cell membrane is negatively charged with respect to the outside when the cell is at rest. When a stimulus is applied to the cell membrane, the selective permeability of the cell membrane is disturbed and it can no longer block the inflow of sodium ions from outside the cell membrane. The inflow of sodium ions at the stimulation site causes the adjacent portions of the cell membrane to lose its selective permeability, thereby causing a chain reaction across the cell membrane until the cell interior is flooded with sodium ions. This process, referred to as depolarization, causes the myocardial cell to have a net positive charge due to the inflow of sodium ions. The electrical depolarization of the cell interior causes a mechanical contraction or shortening of the myofibrils of the cell membrane. The syncytial structure of the myocardium will cause the depolarization originating in any one cell to radiate through the entire mass of the heart muscle so that all cells are stimulated for effective pumping. Following heart contraction or systole, the selective permeability of the cell membrane returns and sodium is pumped out until the cell is repolarized with a negative charge within the cell membrane. This causes the cell membrane to relax and return to the fully extended state, referred to as diastole.
In a normal heart, the sino-atrial (SA) node initiates the myocardial stimulation or "capture" sequence described above. The SA node comprises a bundle of unique cells disposed within the roof of the right atrium. Each cell membrane of the SA node has a characteristic tendency to leak sodium ions gradually over time such that the cell membrane periodically breaks down and allows an inflow of sodium ions, thereby causing the SA node cells to depolarize. The SA node cells are in communication with the surrounding atrial muscle cells such that the depolarization of the SA node cells causes the adjacent atrial muscle cells to depolarize. This results in atrial systole wherein the atria contract to empty blood into the ventricles. The atrial depolarization from the SA node is detected by the atrioventricular (AV) node which, in turn, communicates the depolarization impulse into the ventricles via the Bundle of His and Purkinje fibers following a brief conduction delay. In this fashion, ventricular systole lags behind atrial systole such that the blood from the ventricles is pumped through the body and lungs after being filled by the atria. Atrial and ventricular diastole follow wherein the myocardium is repolarized and the heart muscle relaxed in preparation for the next cardiac cycle. It is when this system fails or functions abnormally that a cardiac pacemaker may be needed to deliver an electronic pacing stimulus for selectively depolarizing the myocardium of the heart so as to maintain proper heart rate and synchronization of the filling and contraction of the atrial and ventricular chambers of the heart.
The success of a cardiac pacemaker in depolarizing or "capturing" the heart hinges on whether the energy of the pacing stimulus as delivered to the myocardium exceeds a threshold value. This threshold value, referred to as the capture threshold, represents the amount of electrical energy required to alter the permeability of the myocardial cells to thereby initiate cell depolarization. If the energy of the pacing stimulus does not exceed the capture threshold, then the permeability of the myocardial cells will not be altered and thus no depolarization will result. If, on the other hand, the energy of the pacing stimulus exceeds the capture threshold, then the permeability of the myocardial cells will be altered such that depolarization will result. Changes in the capture threshold may be detected by monitoring the efficacy of stimulating pulses at a given energy level. If capture does not occur at a particular stimulation energy level which previously was adequate to effect capture, then it can be surmised that the capture threshold has increased and that the stimulation energy should be increased. On the other hand, if capture occurs consistently at a particular stimulation energy level over a relatively large number of successive stimulation cycles, then it is possible that the capture threshold has decreased such that the stimulation energy is being delivered at level higher than necessary to effect capture. This can be verified by lowering the stimulation energy level and monitoring for loss of capture at the new energy level. The ability to detect capture in a pacemaker is extremely desirable in that delivering stimulation pulses having energy far in excess of the patient's capture threshold is wasteful of the pacemaker's limited power supply. In order to minimize current drain on the power supply, it is desirable to automatically adjust the pacemaker such that the amount of stimulation energy delivered to the myocardium is maintained at the lowest level that will reliably capture the heart. To accomplish this, a process known as "capture verification" must be performed wherein the pacemaker monitors to determine whether an evoked depolarization or R-wave occurs in the heart following the delivery of each pacing stimulus pulse.
The prior art is replete with patents which address the problem of polarization voltage or "afterpotentials" hindering capture verification in cardiac pacing systems. U.S. Pat. No. 4,373,531 to Wittkampf et al. teaches the use of pre and post stimulation recharge pulses to neutralize the polarization on the pacing lead. U.S. Pat. No. 4,399,818 to Money teaches the use of a direct-coupled output stage wherein polarization voltages at the heart tissue/electrode interface are dissipated by shorting the electrodes together. U.S. Pat. No. 4,498,478 to Bourgeois teaches the use of a resistor across the output terminals (electrodes) such that a current path is provided for discharging and recharging the effective capacitance at the electrode/tissue interface. U.S. Pat. No. 4,537,201 to Delle-Vedove et al. teaches a linearization of the exponentially decaying sensed signal by applying the sensed signal through an anti-logarithmic amplifier in order to detect a remaining nonlinear component caused by the evoked potential. U.S. Pat. No. 4,674,508 to DeCote, Jr. teaches the use of paired pacing pulses wherein the waveforms sensed through the pacing lead following the generation of each of the pair of pulses are electronically subtracted to yield a difference signal indicative of the evoked cardiac response. U.S. Pat. No. 4,686,988 to Sholder teaches the use of a separate sensing electrode connected to a detector for detecting P-waves in the presence of atrial stimulation pulses, wherein the P-wave detector has an input bandpass characteristic selected to pass frequencies that are associated with P-waves. U.S. Pat. No. 4,821,724 to Whigham et al. teaches the use of a triphasic stimulus having two positive pulses and one negative pulse for balancing the charge at the electrode/tissue interface. U.S. Pat. No. 4,858,610 to Callaghan et al. teaches the use of charge dumping following delivery of the stimulation pulse to decrease lead polarization and also the use of separate pacing and sensing electrodes to eliminate the polarization problem on the sensing electrode. U.S. Pat. No. 5,324,310 to Greeninger et al. teaches the use of the "ring-to-ring" sensing with corresponding atrial and ventricular EGM amplifiers whose outputs are multiplied and compared to a predetermined threshold to determine capture. U.S. Pat. No. 5,486,201 to Canfield discloses an active discharge circuit having a switching device which sequentially and repeatedly couples a charge transfer capacitor to the coupling capacitor to transfer charge therebetween and thereby actively discharge the coupling capacitor.
The foregoing prior art approaches, however, suffer from significant drawbacks. For example, the techniques of the '610 patent to Callaghan and '988 patent to Sholder, which involve using a separate electrode located at some distance from the stimulating electrode for the purpose of isolating the polarization voltages or "afterpotential," are disadvantageous in that they require the additional cost and complexity of the additional sensing electrode. The approaches of the '531 patent to Wittkampf et al. and '508 patent to DeCote, Jr. are unnecessarily wasteful of battery power and unduly complex due to the need to deliver opposite-polarity charges and pairs of closely spaced pacing pulses, respectively, to the electrode. The approach of the '201 patent to Delle-Vedove et al. is similarly disadvantageous in that it requires unnecessarily complex circuitry that it difficult to implement to produce the anti-logarithmic amplifier.
These and numerous other disadvantages of the prior art necessitates the need for the method and apparatus for automatic capture threshold detection provided by the present invention.